Main Ca²⁺ channel triggering ACh release?
P/Q-type (Cav2.1) channels.
These channels are crucial for the release of acetylcholine at the neuromuscular junction.
Effect of low extracellular Ca²⁺?
Increases neuronal excitability (threshold easier to reach).
Low calcium levels can enhance the likelihood of action potentials in neurons.
Presynaptic autoreceptor type?
α3β2 nicotinic receptor.
These receptors play a role in modulating neurotransmitter release.
LEMS target site?
Presynaptic P/Q-type Ca²⁺ channels.
Lambert-Eaton Myasthenic Syndrome affects the release of neurotransmitters at the neuromuscular junction.
MG target site?
Postsynaptic AChRs and end-plate structure.
Myasthenia Gravis primarily affects the receptors that respond to acetylcholine.
Which disease improves with activity?
Lambert-Eaton Myasthenic Syndrome.
Physical activity can enhance neuromuscular transmission in LEMS.
Which disease worsens with activity?
Myasthenia Gravis.
Increased activity can lead to muscle fatigue and weakness in MG.
Drug that prolongs depolarization in LEMS?
3,4-Diaminopyridine (3,4-DAP).
This drug enhances the release of acetylcholine at the neuromuscular junction.
Organ commonly abnormal in MG?
Thymus gland.
The thymus is often involved in the autoimmune process of Myasthenia Gravis.
Trigger for extra-junctional receptor expression?
Denervation or chronic under-stimulation.
These conditions can lead to the formation of receptors outside the normal neuromuscular junction.
Subunit change in fetal receptors?
ε → γ substitution.
This change in subunit composition affects receptor function during development.
Why succinylcholine dangerous in denervation?
Binds extra-junctional γ-receptors → massive K⁺ efflux.
This can lead to severe hyperkalemia and cardiac complications.
Why fetal receptors stay open longer?
Slower closing kinetics and lower conductance.
These properties contribute to prolonged depolarization in fetal muscle.
Why volatile anesthetics can reduce TOF?
They depress muscle excitability and potentiate NM blockade.
This can affect the response to neuromuscular transmission monitoring.
How plasmapheresis helps MG/LEMS?
Removes pathogenic antibodies from plasma.
This treatment can alleviate symptoms by reducing the autoimmune attack on neuromuscular junctions.
